Peoples beliefs are so dependent on viewpoint and focus. All of this represents one part of a much larger picture. Let say you put all the data and knowledge about a subject in a box with holes in it. Now, if you look through one of the holes you see a small part of the picture. Can you then extrapolate the entire picture from your viewpoint? Lets assume, lol, that you can see inside the box and it's not too dark.
As long as you continue looking through that one hole you can justify any belief. Because by narrowing your viewpoint you narrow your evidence and thus clarification seems easier. If the part of the contents of the box you see looks blue you say there is a a blue object inside the box. Never mind that the object is rainbow colored, you will feel quite confident in your assessment of it's color. Until you shift to another hole. Upon which time you will forthrightly insist that the object is orange with a small patch of blue on one side of it!
In nutritional and health related science you have a whole lot of different individuals or groups, each looking through a different hole and many of them convinced that they, and they alone see the truth and why in the hell can't the others see what they see?
When LDL lacks fat and cholesterol, it becomes small and dense (because protein in denser than fat). Such small dense LDL is associated with heart disease because the transporter protein is exposed to glycation and oxidation. Studies show that children eating eggs without the yolk will form the small and dense cholesterol
Not exactly the whole picture. The small dense artherogenic LDL particles versus larger LDL particle thing actually refers to two genetic phenotypes, termed Pattern A and B. B is associated with a prevalence of small dense LDL particles, plasma triglycerides, and reduced levels of HDL. The percentage of the population is hard to pin down and as may be different in different ethnicities. Anywhere from 25 to 35% of white men has been suggested.
This is also called the "atherogenic lipoprotein phenotype".
Although the evidence linking a high fat diet to reductions in small dense LDL as compared to high carbohydrate diets is great it is way early to make broad sweeping conclusions about all this. What is going on is that researchers are trying to determine how, when, and why this phenotype is expressed. So with diet, for instance, is it a reflection of changes in LDL in response to alterations in dietary fat or carbohydrate? And what else is at play?
Those with pattern B would respond differently to a high carbohydrate low fat diet, negatively, than those with "normal" pattern A. And they seem to respond favorably to a high fat diet to a much greater degree than normal subject. Although research is carried out on healthy subjects, hyperlipidemic subjects, etc. this is about research on special populations. It is much too early to come up with a "perfect diet" based on LDL subclass and it is cetainly not justified to say that everybody, across the board will respond the same to carbohydrate.
Also, although studies like to compare extreme opposites, the idea that some people are "recommending" high carbohydrate diets and others recommending high fat diets is what is known as a false dichotomy. These seem to be a prevalent feature in the arguments presented by those who adhere to one agenda. I know of nobody in the nutrition world who recommends a "high carbohydrate diet" which would be a diet that gets the largest percentage of it's calories from carbs. And I know a lot of people in the nutrition world. Likewise the claim that "doctors recommend". This is probably an allusion to the "food pyramid" and it's putting grains on the bottom. The assumption is that everybody else recommends a grain based diet. This is untrue. Categorically untrue.
Given the great variability in human dietary patterns it is a bit difficult to narrow human nutrition down to high carb versus high fat. If you just viewed this based on LDL subclass you still would not be justified in coming to the conclusion that one must consume such a very very high percentage of fat..because it is too early to say that. Research has barely begun. That is another feature of those who focus on one agenda. They seem to see every new development as a huge lightbulb moment and go "wala!" I've got it. When nobody else but them seems to be willing to say that.
But I although some studies compare low carb diets with high fat diets of up to 60% fat we also have here all the glycemic control and high blood sugar stuff. And one is not justified in trying to correlate those two things because glycemic control, although a feature of metabolic syndrome, is not really correlated directly with LDL and dietary lipid reaction.
And when you include all the blood sugar stuff you have to include all the other features that come with that. Like central obesity, insulin resistance, etc. All of which are risk factors of CVD. And is LDL subclass B associated with METs. Yes, high fat diets seem to lower small dense lipoproteins regardless unassociated with weight loss bit this is also always associated with a decrease in total calories on a weight loss inducing diet. And weight loss lowers the risk factors associated with METs.
If you focus all of your research and reading on certain areas you can justify almost anything. It depends on what hole you're looking through. You like fish and hate saturated fat. Then you can cite hundreds of papers to justify that a high fish diet with low saturated fat is more perfect.
Given that, can "pattern B" be induced by a high carbohydrate diet in genetically susceptible people. Yes, I think the evidence is in, pretty much. But will everybody respond the same to a high carbohydrate diet. NO. Should people be consuming high carbohydrate diets? Hell no, lol. Who would recommend this? I certainly wouldn't.
Now, all this focus on this one hole in the box, small dense LDL particles (pattern B) may be ignoring other important data. Let's say that you are put on a cholesterol lowering drug and it "works". Let's say it reduces LDL-C ("low-density lipoprotein cholesterol") and that the cholesterol content of most LDL subfractions were reduced (as this tends to happen), and apolipoprotein B, etc. but let's say that the relative proportion of smaller denser LDL particles were not reduced. In fact let's say their proportion was increased. Is it then justified, based on all evidence, to say that coronary heart disease risk has been increased by the treatment?
That would assume that everyone believes that this is a valid clinical measure of CVD risk and everyone does not. Now, did the authors of this book include any papers that question the validity of this measure in their references? I doubt it. In general this is not a well-established area and it is not yet the standard that some people may make it out to be. Other parameters have been shown to be efficacious as determinants of the success of triglyceride lowering strategies and a corresponding decrease in CVD risk. And this has been shown numerous times. Are some of the studies questionable? Sure. Especially the ones funded by drug companies, lol, which of course would like to establish that LDL subclass is not such an important post treatment parameter since statins do seem to want to raise their proportion and this seems to be significant across the population. But there is lots of data and studies concerning LDL subclass are questionable for many reasons as well.
The authors seem to be implying that it is easy to determine and categorize someone as phenotype B but again, it is not so simple as even if particle size is measured for different analytical methods might produce different results. In other words, the same person may be classified as subtype B by one lab and not subtype B by another. If this phenotype is important clinically, and I think it is based on my limited knowledge, then it needs to be identified consistently but this is not necessarily the case. The authors are taking something with many variables and looking through one hole in the box. Here is a graph to represent this:
LDL Phenotype Classification According to Laboratories Utilizing Different Analytical Methods*. *Lab 1: Pattern B = LDL particle size < 22.0–25.74 nm; AB = 25.75–26.34 nm; Pattern A = 26.3–28.5 nm. Lab 2: Pattern B = LDL particle size ≤20.5 nm; Pattern A = 20.6–22.0 nm. **Significant difference from LAB 1; Χ2 = 64.6, P < 0.0001.
Davy and Davy Lipids in Health and Disease 2006 5:3 doi:10.1186/1476-511X-5-3
So again, even when measuring lab samples, results can vary depending on what hole in the box you're looking through.
The authors also seem to be implying that this subtype does not need to be identified clinically but that an individual should look at the standard, much cheaper measures, looking at among other things LDL number versus HDL number, and extrapolate from there. Which makes no sense. You can't just say, well, there is a correlation between high triglyceride levels and small dense LDL particles so everybody should become an MD and go extrapolating from their lab results even though their doctor did not order, nor would their insurance pay for an actual clinical count. And without actual clinical counts you can't get a reliable data-set to correlate small dense particle number with CVD risk. If something is clinically relevant it needs to be clinically measured.
It is not proper to imply that LKL cholesterol, etc. measured by standard tests are predictive in terms of these new parameters. Because this has not been shown. Clinical trials would have to be carried out comparing standard tests versus better tests for LDL particle size and apolipoprotein_B would be needed. And then of course there is the issue of standardization. At least with ApoB there is a reference material I was able to find that is considered good, developed by WHO, CDC and the IFCC called SP3-07. Labs would need to conform to this reference standard to reduce the variability among the different methods.
On the egg white thing. One very important thing is that not all individuals respond the same to cholesterol in the diet or lack thereof. To say that everybody who eats egg whites will experience an increase in small dense LDL particles and a decrease in large ones is not justified. Likewise to say that everyone who eats eggs will see a decrease in small dense particles and an increase in large one is not justified. Some people will see hardly any response in ldl or hdl period, as compared to other "hyper-responders". To try to come up with a "perfect diet" you first have to believe that everybody, or at least a significant portion, of the population respond the same to the same diet, and this is a ridiculous notion, despite the idea that "some people can handle" this or that. which is not data but a vague disclaimer.
Here is one paper to read: